Effect of duodenum-preserving resection of the head of the pancreas on endocrine and exocrine pancreatic function in patients with chronic pancreatitis

Two mobilizable cloning vectors, designated pABW1 and pAWB2, were constructed basing on the E. coli vector pBGS18 and oriT originating from RK2. In pABW2 the kanamycin resistance gene was replaced by a novel tetracycline resistance cassette derived from Tn1721. Both vectors, specific for E. coli, allow to perform the cloning steps in E. coli and then to efficiently transfer the constructs by conjugation to the host of choice. A vector which cannot propagate in the given host can be applied for identification of the host specific plasmid replicator regions. With the use of pABW2 we defined the minimal replicator region of pTAV202-a mini-derivative of the large pTAV1 plasmid of P. versutus. We also proved that RepC' encoded on this fragment is the principal initiator replication protein and that oriV is located along its coding sequence.     

MRI of primary malignant cardiovascular tumors

In 1895 Trendelenburg described his sign to determine the integrity of hip function. We found the sign to be positive in a patient whose hip was clinically and radiologically normal, and therefore investigated this in other patients. We confirmed that a medial shift of the mechanical axis of the leg below the hip may cause a positive Trendelenburg sign. This has not been previously described.     

Behavioral and pharmacologic approaches to smoking cessation

Cigarette smoking continues to be the single, most preventable cause of death and disability in the United States. For individuals who have cancer, continuing to smoke negatively impacts their treatment, survival, and risk for second primary tumors. This review of behavioral and pharmacological approaches to smoking cessation focuses on the recent comprehensive review of cessation interventions by the Agency for Health Care Policy and Research (AHCPR), as well as on new developments in the field. An intervention model is outlined that provides oncologists with a brief and easily implemented method of systematically treating patients who smoke. By assessing patient smoking status, advising smoking patients to quit, and proactively assisting their patients in quitting, oncologists can significantly influence patient health and fulfill their professional and ethical responsibility to address this life-threatening behavior.     

Transgenic overproduction of islet amyloid polypeptide (amylin) is not sufficient for islet amyloid formation

Islet amyloid polypeptide forms islet amyloid deposits in non-insulin-dependent diabetes mellitus. We have generated transgenic mice which express human islet amyloid polypeptide in their pancreatic beta cells yet do not develop islet amyloid deposits despite producing levels of the amyloidogenic human peptide 2 - 3 fold higher than the native (mouse) peptide. To determine whether marked overproduction of islet amyloid polypeptide is a potential cause of islet amyloid formation, we increased expression of this transgene by producing homozygous transgenic animals and by making heterozygous mice experimentally insulin resistant with nicotinic acid. Pancreatic content of islet amyloid polypeptide-like immunoreactivity in homozygous and nicotinic acid-treated mice was 2-fold (25 +/- 7 fmol/microg; n = 6) and 3.5-fold (47 +/- 20 fmol/microg; n = 3) higher, respectively, than that of untreated heterozygous animals (13+/-2 fmol/microg; n = 11; both p < 0.05). Despite this marked increase in production of islet amyloid polypeptide, neither group of mice developed gross islet amyloid deposits even after 16 months of age. We conclude that overproduction of islet amyloid polypeptide, even as produced by extreme insulin resistance, is not in itself sufficient for islet amyloid formation.     

Evaluation of serum gamma-glutamyltransferase activity as a predictor of passive transfer status in crias

OBJECTIVE: To determine the relationship between serum gamma-glutamyltransferase (GGT) activity and serum IgG concentration in neonatal crias. DESIGN: Prospective observational study. ANIMALS: 21 llama and 4 alpaca crias from 0 to 5 days old. PROCEDURE: Serum GGT activity was measured, using a commercially available kit. Serum IgG concentration was determined by use of radial immunodiffusion. With a serum IgG concentration of 1,000 mg/dl (considered adequate passive transfer), specificity and sensitivity of serum GGT activity in the detection of failure of passive transfer were determined. Regression models were developed to determine the relationship between serum GGT activity and serum IgG concentration. RESULTS: Sensitivity ranged from 0.56 to 0.89, and specificity ranged from 0.88 to 0.31, depending on the value of serum GGT activity chosen as a threshold. Proportion of crias correctly classified ranged from 0.76 to 0.52. Regression models failed to demonstrate a significant relationship between serum GGT activity and serum IgG concentration. CLINICAL IMPLICATIONS: Passive transfer status in crias cannot be accurately predicted on the basis of serum GGT activity.     

Patterns of DSM-III-R alcohol dependence symptom progression in a general population survey

Age of onset reports obtained retrospectively for each symptom of DSM-III-R alcohol dependence (AD) are used to study patterns of lifetime symptom progression in a large general-population survey of people in the United States. It is shown that symptom progression among a substantial majority of respondents can be summarized as movement across three clusters. Cluster A is defined by symptoms of role impairment/hazardous use (A4), use despite social, psychological or physical problems (A6), and drinking larger amounts or over a longer period of time than intended (A1). Cluster B is defined by tolerance (A7) and impaired control (A2, A3). Cluster C is defined by withdrawal (A8, A9) and giving up activities in order to drink (A5). Clusters are shown to follow a time sequence, with at least one symptom in Cluster A usually occurring first, followed by symptoms in Clusters B and C. In all, 83.4% of the symptom cluster transitions estimated from retrospective age of onset reports are consistent with this progression. Progression to AD is differentially predicted by symptom profiles reported at the age of first symptom onset, with persons reporting Cluster C symptoms most likely to progress subsequently to AD. Furthermore, profiles of AD defined by the highest symptom cluster present at AD onset are differentially predicted by prior personal and parental histories of psychopathology and, among men, are predictive of diagnosis persistence.